Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Physiology > Module 2: Lecture 5 > Flashcards

Module 2: Lecture 5 Flashcards

1
Q

What is the most important immune reaction?

A

inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Which responses will activate quicker? Innate or adaptive?

A

innate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

How long does it normally take for an innate response to activate?

A

within minutes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is the peak activation for innate responses regarding the chart?

A

2-3 days

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is the peak activation for adaptive responses regarding the chart?

A

7 days give or take

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

True or False
We need innate responses to activate adaptive responses?

A

true

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is inflammation?

A
  • occurs every time, everywhere there is an infection
  • it’s an INNATE response that it is a nonspecfic to tissue injury
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What happens when there is inflammation?
Using an example of damage to the skin

A

AT THE SITE OF INFECTION:
1. Macrophages (Resident immune cells) are the cells that are first alerted of the presence of pathogen or injury

  1. macrophages will go through phagocytosis to remove dead/damaged cells, then they call for backup
  2. Then they release cytokine, chemokines and others, they will activate nearby immune cells called mast cells (other resident immune cells)
  3. Mast cells will release their mediators including histamines
  4. cytokines and histamine will act on the endothelial cells that are lining the blood vessel (which Is narrow) and force it to dilate (localized vasodilation) for more flow in that region (only in the local site of infection)
  5. It allows the endothelial cells lining the blood vessel to have a tiny space between them, allowing the immune cells in the blood to squeeze through and exit to the site of infection.
  6. finally clotting factors are activated
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is the goal of inflammation?

A
  • get rid of a pathogen if it’s bacterial-related
  • REPAIR the tissue damage
  • regenerate the tissue
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

True or False
Every tissue has resident immune cells aka macrophages?

A

true

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are the three roles of macrophages at the site of infection during inflammation?

A
  • isolate
  • destroy
  • inactivate the invader
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what is emigration?

A

recruitment of leukocytes aka neutrophils and monocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

True or False
Cells never come to the site of infection via lymph it is always through the bloodstream

A

True

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

in the inflammatory phase of the immune response while WBCs do NOT exit the blood?

A

t-cells and b-cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Which WBC will come from the blood first?

A

neutrophils

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Which two plasma proteins will come help at the site of infection from the blood?

A
  1. complement proteins (innate responses process)
  2. gamma globulins (antibodies)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What do complement proteins do at the site of infection?

A

they will bind, and stick to the surface of pathogens and ONLY pathogens

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

How do complement proteins know to attach to the pathogens?

A
  • via sugar molecules
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is the job of complement proteins after they stick to a pathogen?

A
  • either punch holes in the surface of the pathogen and kill them
  • allow our immune cells to phagocytosis them better

*non-specific innate response which allows for the destruction of the bacteria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What do cytokines do?

A
  • allow cell movement, attack other cells (chemokines)
  • can directly kill a pathogen (not very common)
  • they can raise the temperature (locally causing muscle and some fat deposits to start burning their glucose to generate heat rather than making ATP) (just changing the metabolism)
  • eventually, they go from local to systemic which will cause a fever
  • fever is good because pathogens cannot replicate under certain temperatures
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is the difference between local and systemic?

A
  • local, is localizing a change in one part of the body
  • systemic is changing the entire body system
22
Q

What are the three most powerful cytokines?

A
  1. Interleukin (IL)-1,6 and TNF
  • they increase the body temperature to cause fever
  • they lower the plasma concentration aka the iron concentration, so bacteria cannot grow by using iron molecules as a result they do not get delivered to the tissues as much
  • they act on the liver to release acute-phase proteins (systemic function), they are inflammatory proteins that will cause inflammation

ie. CRP (if there is a high level of this in our blood we will know that we have an active inflammation internally)

  • they can activate blood clotting to seal off infected areas
23
Q

Which tissue can we not regenerate? and what can we do instead?

A
  • muscle tissue and nerve tissue
  • we stuff it with collagen
24
Q

What is aberrant or inappropriate inflmmatory responses

A

overreaction to a pathogen to out injury

25
Q

What is an auto-inflammatory response

A

when we activate inflammatory responses against our tissue

26
Q

What is a low-grade inflammation response?

A

caused by metabolic dysfunction, aka eating too much sugar

27
Q

Over time what can chronic inflammation responses cause?

A
  • Alzheimers
  • Atherosclerosis
  • Heart disease
  • Allergic reactions
  • Type 2 diabetes
  • Cancer
28
Q

What can we take for an over-inflammatory reaction?

A
  • nonsteroidal anti-inflammatory drugs (NSAIDs)
    ie. tylenol, Advil
  • glucocorticoids steroids (if you have to)
  • have things that can block our most powerful cytokines
29
Q

What is the other response other than inflammation when there are pathogens?

A

antiviral responses

30
Q

When do we use antiviral responses?

A

if the virus is inside the cell we cannot do phagocytosis

31
Q

What can we do when there is a virus in our cells?

A
  • we activate things called interferons (a kind of cytokine) which will activate a large program of gene transcription in the cell and prevent or limit the spread of the virus
  • they can cause a cell that is infected to kill itself and self-destruct or it can cause it to stop making more protein so it stops making more viruses of those kind
32
Q

What is the complement system?

A

made by: liver
- normally they are inactive

  • when there’s a pathogen and we have inflammation, they leak into the site of infection
  • they see a pathogen and then are activated by three mechanisms
  1. spontaneously
    - sticks to the surface of the pathogen, identifies it’s a pathogen and then gets activated
  2. sugar molecules on the surface of the pathogen
    - these sugar molecules are arranged specifically, so the complement proteins will recognize that and get activated
  3. antibodies (most time-consuming)
    made by: b cells
    - they can activate complements proteins
  • antibodies will take the longest for activation as they are made by adaptive cells which we know takes more time

AFTER THEY ARE ACTIVATED and now two things happen

  1. membrane attack complement (MAC)
    - punch a hole in the surface of the pathogen
    - everything leaks out and it dies
  2. phagocytes via receptor-mediated endocytosis
    - they coat the pathogen
    - and then phagocytosis, but some pathogens can escape this method
    - once they coat the pathogen, macrophages and all phagocytes have receptors for complement proteins, now they can help/enhance phagocytosis
33
Q

True or False
All plasma proteins are made by the liver except gamma globulins

A

true

34
Q

What are Dendritic Cells (DC)

A
  • resident immune cells
  • not important for initial inflammatory response nevertheless still very important
  • they do macropinocytosis
    immature: in tissues
    mature: encounters a pathogen
35
Q

What is the job name of Dendritic Cells (DC)?

A

antigen-presenting cells

36
Q

Overall what is our MOST powerful immune cell?

A

T-CELL

37
Q

What are the steps of how Dendritic Cells work?

A
  1. immature DC reside in peripheral tissue
  2. DC cells migrate via lymphatic vessels to regional lymph nodes
  3. Mature DC activate T-Cells in lymphoid organs such as lymph nodes
38
Q

What are the most important cells in activating inflammation?

A

macrophages

39
Q

Macrophages release what at the site of an infection/injury?

A

cytokine, chemokines

40
Q

what do cytokines, chemokines do after being made and released by macrophages at the site of infection/ injury?

A
  • they activate other nearby mast cells (resident immune cells)
41
Q

What do mast cells release?

A
  • their mediators
  • histamine
42
Q

What do cytokines and histamine do after being released?

A
  • they will act on endothelial cells that are in the lining of the blood vessels to make gaps in between them allowing the immune cells in the bloodstream to squeeze out and go to the site of infection
43
Q

Why would other fluids and plasma proteins leak outside of the bloodstream?

A

because of the lack of colloidal pressure opposing the osmotic pressure

44
Q

What is the cause of edema at the site of infection/injury?

A

all the pressure from the WBC going towards the site of infection

45
Q

What causes pain at the site of infection/injury?

A

the pressure of all the WBC hitting the pain receptors

46
Q

What causes the redness at the site of infection/injury?

A

some of the rbc will leak out of the bloodstream

47
Q

What causes the heat at the site of infection/injury?

A

cytokine will increase the temperature via burning the glucose from some muscle and fat deposits to generate heat rather than making ATP

48
Q

Can complement proteins go into the cell

A

NO

49
Q

After the complement proteins are activated what are the two ways they can fulfil their job?

A
  1. membrane attack complement (MAC)
    - punch a hole in the surface of the pathogen
    - everything leaks out and it dies
  2. phagocytes via receptor-mediated endocytosis
    - they coat the pathogen
    - and then phagocytosis, but some pathogens can escape this method
    - once they coat the pathogen, macrophages and all phagocytes have receptors for complement proteins, now they can help/enhance phagocytosis
50
Q

What are the three ways the complement system can become activated?

A
  1. spontaneously
    - sticks to the surface of the pathogen, identifies it’s a pathogen and then gets activated
  2. sugar molecules on the surface of the pathogen
    - these sugar molecules are arranged specifically, so the complement proteins will recognize that and get activated
  3. antibodies (most time-consuming)
    made by: b cells
    - they can activate complements proteins
51
Q

Which of the three ways to activate the complement system will take the longest?

A

antibodies will take the longest for activation as they are made by adaptive cells which we know takes more time

Physiology (27 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions